Switching on the Lights: The Use of Optogenetics to Advance Retinal Gene Therapy

Abstract

Photoreceptors carry a high number of mitochondria necessary to maintain their high metabolic rate. This allows them to respond rapidly to small changes in illumination. However, the metabolically demanding role of light reception appears to render photoreceptors particularly vulnerable to mutations; this is manifested in the many clinical forms of hereditary retinal degeneration (RD).1 Remarkably, in many cases the remainder of the retinal circuitry remains capable of firing despite the death of the photoreceptor cells.2,3 In this issue of Molecular Therapy, Caporale et al. exploit this residual capacity for signal transmission so as to endow retinal ganglion cells with the ability to take over the task of light detection from the photoreceptors in conditions of RD.4